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Melanoma GEMM Tumors, untreated or vemurafenib treated [bulk RNA-seq]

ABSTRACT: Melanoma GEMM Tumors, untreated or vemurafenib treated [bulk RNA-seq]

PROVIDER: PRJNA844272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19502500.fastq.gz	Fastqsanger.gz
	SRR19502501.fastq.gz	Fastqsanger.gz
	SRR19502468.fastq.gz	Fastqsanger.gz
	SRR19502469.fastq.gz	Fastqsanger.gz
	SRR19502470.fastq.gz	Fastqsanger.gz

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Melanoma GEMM Tumors, untreated or vemurafenib treated

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Project description:Emerging research suggests that multiple tumor compartments can influence treatment responsiveness and relapse, yet the search for therapeutic resistance mechanisms remains largely focused on acquired genomic alterations in cancer cells. Here, we show how treatment-induced changes occur in multiple tumor compartments during tumor relapse and can reduce benefit of follow-on therapies. By utilizing serial biopsies, next generation sequencing and single cell transcriptomics, we tracked the evolution of multiple cellular compartments within individual lesions during first-line treatment response, relapse and second-line therapeutic interventions in an autochthonous model of melanoma. We discovered that while treatment-relapsed tumors remained genetically stable, they converged on a shared resistance phenotype characterized by dramatic changes in tumor cell differentiation state, immune infiltration and extracellular matrix (ECM) composition. Similar alterations in tumor cell differentiation were also observed in more than half of our treatment-relapsed patient tumors. Tumor cell state changes were coincident with ECM remodeling and increased tumor stiffness, which alone was sufficient to alter tumor cell fate and reduce treatment responses in melanoma cell lines in vitro. Despite the absence of acquired mutations in the targeted pathway, resistant tumors showed significantly decreased responsiveness to second-line therapy intervention within the same pathway. The ability to preclinically model relapse and refractory settings - while capturing dynamics within and crosstalk between all relevant tumor compartments - provides a unique opportunity to better design and sequence appropriate clinical interventions.

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Melanoma GEMM Tumors, untreated or vemurafenib treated

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-01 | GSE205294 | GEO

Vemurafenib induces a noncanonical senescence-associated secretory phenotype in melanoma cells which promotes vemurafenib resistance

Project description:To explore the characteristics of senescent melanoma cells induced by vemurafenib or cisplatin, melanoma A375 cells were treated with vemurafenib and cisplatin, respectively. The senescent phenotypes were verified by β-gal staining, EdU assay, cell morphology and the senescence-related pathways. RNA-seq was performed to explore the differentially expressed genes in the senescent cells induced by vemurafenib or cisplatin.

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Project description:The BRAFV600E mutant melanoma cell line M14 responds to the BRAF inhibitor vemurafenib, however, the differences in response between individual cells are underlying resistance. To highlight the underlying mechanisms, we performed treatment of M14 cells with vemurafenib, followed by Drop-seq. We were able to clearly distinguish cells that were treated with the drug from untreated cells, and we discovered different cell populations within the treated cells, likely reflecting heterogeneity of drug resistant cells. We were able to identify specific biomarkers, as preferentially expressed genes, for each cell population. The results of our study will address preexisting and acquired drug resistance that limits clinical usefulness of targeted strategies.

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Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

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Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

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